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PM · Lens · The Effect of Apigenin on Renal Damage Induced by Aristolochic Acid I and the Involvement of Nrf2/HO-1 Pathway

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Article · Volume 21, Issue 2 · pp. 599–607

The Effect of Apigenin on Renal Damage Induced by Aristolochic Acid I and the Involvement of Nrf2/HO-1 Pathway

Leyi Ma1, Zijiao Quan2, Nan Zheng3, Ming Lin4

  1. 1Department of Urinary Surgery, Yongjia People’s Hospital, Wenzhou, Zhejiang, China.
  2. 2Wenzhou University, Wenzhou, Zhejiang, China.
  3. 3College of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  4. 4Department of Nephrology, Cangnan Hospital Affiliated to Wenzhou Medical University, Wenzhou, Zhejiang, China.

Abstract

Background: Aristolochic acid is naturally found in plants of the Aristolochiaceae family and possesses antitumor, antiinfection, and anti-inflammatory properties.Objectives: This study investigated the protective effect of apigenin (API) on aristolochic acid I (AAI)-induced renal damage in mice and its underlying mechanisms.Materials and Methods: Male C57BL/6J mice were assigned to the control group, model group, and API low, medium, and high-dose groups (10, 20, 40 mg/kg). On the 5th day, 2 h after administration, except for the control group, all other groups were intraperitoneally injected with AAI (10 mg/kg). Following final administration, 24-h urinary protein levels, serum creatinine (Scr), and blood urea nitrogen (BUN) levels were assessed along with hematoxylin–eosin (HE) staining of kidneys and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, as well as analysis of malondialdehyde (MDA) levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity.Results: When compared with the model group, mice in API treatment groups exhibited significantly reduced 24-h urinary protein levels and serum levels of Scr and BUN (p < 0.05) with an improvement in renal tissue histopathological changes and cell apoptosis as well as decreased MDA and increased SOD and GSH-Px (p < 0.05). Tumor necrosis factor alpha protein (TNF-α)/interleukin (IL)-1β/IL-6 levels showed a reduction (p < 0.05). Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were upregulated, while NF-κB/Cleaved Caspase-3 were downregulated (p < 0.01).Conclusion: API protects against renal damage induced by AAI possibly through Nrf2/HO-1 pathway, which in turn inhibits oxidative stress damage, inflammatory responses, and cell apoptosis.

Keywords: Apigenin; aristolochic acid I; renal damage; nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway

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